RESUMEN
We investigated to determine why heating of squid muscle at 60 degrees C induced the liberation of actin from myofibrils. When a mixture of a myofibrillar fraction and a low-molecular sarcoplasmic fraction prepared from squid muscle was heated at 60 degrees C, actin liberation occurred. When a myofibrillar fraction was heated with ATP, AMP, or IMP, actin liberation occurred. Hence, AMP is perhaps one of the factors causing actin liberation in postmortem squid muscle. It was found that AMP and IMP reversibly dissociated actomyosin of chicken, bovine, and porcine skeletal muscles into actin and myosin on incubation at 0 degrees C at pH 7.2 in 0.2 M KCl. These results led us to conclude that AMP and IMP were the most responsible factors causing actin liberation from myofibrils in the heated muscle and causing reversible dissociation of actomyosin on storage of skeletal muscle at a low temperature. Hence, AMP and IMP are possible factors causing the resolution of rigor mortis in muscles.
Asunto(s)
Actinas/metabolismo , Actomiosina/metabolismo , Adenosina Monofosfato/metabolismo , Inosina Monofosfato/metabolismo , Miosinas/metabolismo , Animales , Decapodiformes/metabolismo , Calor , Peso MolecularRESUMEN
The extraordinary Hall resistivity rho(xy) and the magnetization M of a canonical spin glass AuFe (8 at.% Fe) were measured simultaneously as functions of temperature with the best care to the thermal and the magnetic field hysteresis. The data of rho(xy) show an anomaly at the spin glass transition temperature T(g) and have different zero field cooling (ZFC) and field cooling (FC) measurements below T(g). Moreover, the value of rho(xy)/M, which represents the chiral susceptibility of the system in the present case, also shows the difference between ZFC and FC measurements. The results are consistent with the predictions of the chirality scenario of canonical spin glasses by Kawamura.
RESUMEN
This report documents the clinical, radiographic and histologic findings in a 46-year-old man with calcifying tendinitis in his left shoulder which progressed to rotator cuff tear. The patient had a 1-year history of repeated calcifying tendinitis before being referred to our hospital. On the initial visit, radiographs and magnetic resonance imaging (MRI) revealed calcium deposition localized in the supraspinatus tendon without apparent tear. Three months after the first visit, MRI revealed a partial-thickness rotator cuff tear at the site of calcium deposition. Surgical and histologic findings demonstrated that calcium deposition was the cause of cuff rupture. To our knowledge, based on a review of the English literature, this is the first case report in which the progression from calcifying tendinitis to rotator cuff tear has been serially observed.